1. Field of the Invention
The present invention relates to the field of glaucoma. More specifically, the invention provides a method to protect glaucomatous retinopathy using compositions comprising at least one non-feminizing estrogen.
2. Description of the Related Art
“Glaucomas” are a group of debilitating eye diseases that are the leading cause of preventable blindness in the United States and other developed nations. Primary Open Angle Glaucoma (POAG) is the most common form of glaucoma. The disease is characterized by the degeneration of the trabecular meshwork (TM), leading to obstruction of the normal ability of aqueous humor to leave the eye without closure of the space (e.g., the “angle”) between the iris and cornea (Langham (1979); Segawa (1979); Rohen (1983)). A characteristic of such obstruction in this disease is an increased intraocular pressure (IOP), resulting in progressive visual loss and blindness if not treated appropriately and in a timely fashion. The disease is estimated to affect between 0.4% and 3.3% of all adults over 40 years old (Leske et al. (1994, 1997, 2001); Bengtsson (1989); Strong (1992)). Moreover, the prevalence of the disease rises with age to over 6% of those 75 years or older (Strong (1992)).
Another form of POAG, normal-tension glaucoma, is characterized by a severe optic neuropathy in the absence of abnormally high IOP. Patients with normal-tension glaucoma have pressures within the normal range, albeit often in the high normal range (Tanna & Jampel (2000)).
Because increased IOP is a readily measurable characteristic of glaucoma, the diagnosis of the disease is largely based on an increase in IOP which is generally estimated by tonometry (Strong (1992); Greve & Chisholm (1993)). Unfortunately, as is evident from normal-tension glaucoma, glaucomatous retinopathy and optic nerve damage can occur in the absence of abnormally high IOP (Yamamoto & Kitazawa (1998); Tanna & Jampel (2000)). Conversely, ocular hypertension does not always lead directly to retina or optic nerve damage. Approximately 5 million Americans have elevated IOP without optic nerve damage or visual field loss. Because the relationship between pressure and optic nerve and retina damage is not necessarily direct, high IOP is now considered to be only a risk factor rather than an essential disease characteristic. For this reason, additional methods, such as direct examination of the optic disk and determination of the extent of a patient's visual field loss are often conducted to improve the accuracy of diagnosis (Greve & Chisholm (1993)). Also for the same reason, the ultimate goal of glaucoma treatment is to preserve vision by protecting against the pathological changes in the retina and optic nerve.
Current glaucoma therapy is directed to lowering IOP. A variety of therapeutic agents have been proposed as having the ability to reduce elevated IOP. These therapies lower IOP, but they do not directly address the pathogenic mechanisms occurring at the retina and optic nerve, and the disease continues to progress. Moreover, many of these agents are often associated with untoward effects. There is currently no generally accepted therapeutic method to manage glaucomatous retinopathy and optic neuropathy. Agents offering retinoprotection properties would be desirable.